Dpm. Van Den Bogaert et al., The continuous 7-hour intravenous dexamethasone suppression test in the differential diagnosis of ACTH-dependent Gushing's syndrome, CLIN ENDOCR, 51(2), 1999, pp. 193-198
OBJECTIVE A recent report showing disappointingly low sensitivity and speci
ficity for the oral high dose dexamethasone test in the differential diagno
sis of Gushing's syndrome prompted us to re-evaluate the results obtained i
n our centre using the continuous 7-hour intravenous dexamethasone suppress
ion test for this purpose.
PATIENTS 105 patients with AGTH-dependent Gushing's syndrome were included
in this study; 78 with Gushing's disease, 8 with ectopic ACTH-secreting tum
ours and 19 were classified as 'of unknown aetiology'.
RESULTS In 74/78 (94.9%) of patients with Gushing's disease and in 3/8 (37.
5%) patients with the ectopic ACTH syndrome, a plasma cortisol decrease >19
0 nmol/l at 7 h as compared to baseline values was achieved in the continuo
us 7-hour intravenous dexamethasone suppression test. Using a plasma cortis
ol decrease >190 nmol/l at 7 h as compared to baseline values as the cut-of
f value, the sensitivity and specificity of the continuous 7-hour intraveno
us dexamethasone suppression test for the diagnosis of Gushing's disease in
patients with AGTH-dependent Gushing's syndrome were 94.9% and 62.5%, resp
ectively.
CONCLUSIONS In patients with AGTH-dependent Gushing's syndrome with a plasm
a cortisol decrease >190 nmol/l at 7 h in the continuous 7-hour intravenous
dexamethasone suppression test, additional localizing investigations such
as bilateral simultaneous inferior petrosal sinus sampling and/or pentetreo
tide scintigraphy should be performed when no clearly discernible pituitary
adenoma is observed on MRI studies. Patients with ACTH-dependent Gushing's
syndrome with a plasma cortisol decrease <190 nmol/l at 7 h in the continu
ous 7-hour intravenous dexamethasone suppression test should also undergo b
ilateral simultaneous inferior petrosal sinus sampling and/or pentetreotide
scintigraphy to demonstrate the presence of a nonpituitary source of ACTH
overproduction.